PMID- 7882594
OWN - NLM
STAT- MEDLINE
DCOM- 19950411
LR  - 20190821
IS  - 0090-1229 (Print)
IS  - 0090-1229 (Linking)
VI  - 75
IP  - 1
DP  - 1995 Apr
TI  - Role of TNF alpha, IL-1, and IL-1ra in the mediation of leukocyte infiltration 
      and increased vascular permeability in rabbits with LPS-induced pleurisy.
PG  - 68-74
AB  - We examined the generation of tumor necrosis factor-alpha (TNF alpha), 
      interleukin-1 (IL-1), and IL-1 receptor antagonist (IL-1ra), and their role in 
      the mediation of leukocyte infiltration and increased vascular permeability in 
      rabbits with LPS-induced pleurisy. The leukocyte infiltration was largely 
      mediated by both TNF alpha and IL-1 and could be divided into at least two 
      phases: the early (within 3 hr) phase which was partly inhibited by anti-TNF 
      alpha, but not by IL-1ra, and the late phase (4-12 hr) mediated by both TNF alpha 
      and IL-1, and largely inhibited synergistically with anti-TNF alpha and IL-1ra. 
      Endogenous IL-1ra may be responsible for the downregulation of the late phase of 
      leukocyte infiltration in this type of inflammation. The increased vascular 
      permeability was composed of two phases: immediate (15 min) and delayed (2 hr). 
      The immediate permeability was inhibited by H1-antihistamine but was not affected 
      by anti-TNF alpha, by IL-1ra, or by depletion of neutrophils. The delayed 
      permeability was completely inhibited by either depletion of neutrophils or by 
      anti-TNF alpha and was not affected by IL-1ra or antihistamine. Production of TNF 
      alpha was maintained in the leukopenic rabbits. It would thus appear that the 
      delayed permeability is mediated by a relatively early fraction of leukocyte 
      infiltration initiated by TNF alpha; however, TNF alpha is not the direct 
      mediator of this delayed permeability.
FAU - Edamitsu, S
AU  - Edamitsu S
AD  - Department of Pathology, Kumamoto University School of Medicine, Japan.
FAU - Matsukawa, A
AU  - Matsukawa A
FAU - Ohkawara, S
AU  - Ohkawara S
FAU - Takagi, K
AU  - Takagi K
FAU - Nariuchi, H
AU  - Nariuchi H
FAU - Yoshinaga, M
AU  - Yoshinaga M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Clin Immunol Immunopathol
JT  - Clinical immunology and immunopathology
JID - 0356637
RN  - 0 (Antibodies)
RN  - 0 (Interleukin-1)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Receptors, Interleukin-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 2L8T9S52QM (Triprolidine)
SB  - IM
MH  - Animals
MH  - Antibodies/pharmacology
MH  - Capillary Permeability/drug effects/*physiology
MH  - Interleukin-1/biosynthesis/*physiology
MH  - Leukocytes/*physiology
MH  - Lipopolysaccharides
MH  - Pleura/cytology
MH  - Pleurisy/*chemically induced/metabolism/*physiopathology
MH  - Rabbits
MH  - Receptors, Interleukin-1/*antagonists & inhibitors/metabolism/physiology
MH  - Triprolidine/pharmacology
MH  - Tumor Necrosis Factor-alpha/immunology/*physiology
EDAT- 1995/04/01 00:00
MHDA- 1995/04/01 00:01
CRDT- 1995/04/01 00:00
PHST- 1995/04/01 00:00 [pubmed]
PHST- 1995/04/01 00:01 [medline]
PHST- 1995/04/01 00:00 [entrez]
AID - S0090122985710549 [pii]
AID - 10.1006/clin.1995.1054 [doi]
PST - ppublish
SO  - Clin Immunol Immunopathol. 1995 Apr;75(1):68-74. doi: 10.1006/clin.1995.1054.